AI Article Synopsis
- Proper assembly and maintenance of epithelia are crucial for normal development, and the B1 isoform of the ecdysone receptor (EcR-B1) plays a key role in this process, specifically in the Drosophila ovary model.
- Silencing the EcR-B1 receptor leads to loss of integrity in the follicular epithelium, resulting in multilayering and disrupted cell polarity, evidenced by altered distributions of cell polarity markers like aPKC and Dlg.
- The study reveals that EcR-B1 is essential for maintaining proper follicle cell polarity during various stages of oogenesis and for ensuring follicle cell survival, with its dysfunction leading to cell death through caspase activation.
Article Abstract
Proper assembly and maintenance of epithelia are critical for normal development and homeostasis. Here, using the Drosophila ovary as a model, we identify a role for the B1 isoform of the ecdysone receptor (EcR-B1) in this process. We performed a reverse genetic analysis of EcR-B1 function during oogenesis and demonstrate that silencing of this receptor isoform causes loss of integrity and multilayering of the follicular epithelium. We show that multilayered follicle cells lack proper cell polarity with altered distribution of apical and basolateral cell polarity markers including atypical-protein kinase C (aPKC), Discs-large (Dlg), and Scribble (Scrib) and aberrant accumulation of adherens junctions and F-actin cytoskeleton. We find that the EcR-B1 isoform is required for proper follicle cell polarity both during early stages of oogenesis, when follicle cells undergo the mitotic cell cycle, and at midoogenesis when these cells stop dividing and undergo several endocycles. In addition, we show that the EcR-B1 isoform is required during early oogenesis for follicle cell survival and that disruption of its function causes apoptotic cell death induced by caspase.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2621165 | PMC |
| http://dx.doi.org/10.1534/genetics.108.096008 | DOI Listing |
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